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Potassium Disorders

Potassium Disorders

JULY 2003  VOL 5.6

Peer Reviewed

Editorial Mission Disorders To provide busy practitioners with concise, peer-reviewed recommendations Thomas Schermerhorn, VMD, DACVIM on current treatment standards drawn from Assistant Professor, Small Animal Medicine published veterinary medical literature. Deborah Hall-Fonte, DVM Resident in Small Animal Medicine

College of Veterinary Medicine This publication acknowledges that Kansas State University standards may vary according to individual Manhattan, Kansas experience and practices or regional otassium is important for nearly every physiologic function as a crucial constituent differences. The publisher is not responsible of the intracellular and compartments. Potassium is essential for for author errors. Pnormal function of nervous, cardiac, and muscle tissue and plays a vital role in the renal, gastrointestinal (GI), and endocrine systems. Multiple regulatory systems operate Reviewed 2015 for significant advances concurrently to maintain potassium balance within precise physiologic limits in normal in medicine since the date of original dogs and cats (Table 1). There are numerous pathologic processes and disease states that publication. No revisions have been derange potassium . Some of these are primary disorders of potassium balance, made to the original text. but others alter potassium balance indirectly as a consequence of a general pathologic change (secondary potassium disorders). As a result, potassium abnormalities are probably the most common—and most significant—of the changes encountered in Executive Series Editor daily practice. For this reason, prompt recognition and correction of potassium imbalance in sick animals will reduce morbidity and improve treatment outcomes for many patients. Richard B. Ford, DVM, MS Potassium imbalance can occur in association with a large number of disorders, and complete discussion of each of these disorders is beyond the scope of this article. Two Editor in Chief important primary potassium disorders, hypoadrenocorticism (Addison’s disease) and Beth Thompson, VMD hyperaldosteronism (Conn’s syndrome), will be discussed in detail. Relevant general information about the clinical management of potassium imbalances will also be presented. Editorial Review Board Nishi Dhupa, DVM, DACVECC DIAGNOSTIC CRITERIA Cornell University Historical Information Cynthia Otto, DVM, DACVECC University of Pennsylvania Gender Predisposition Overall, there is no gender predisposition for potassium disorders. Mark Rubash, DVM, DACVECC ••Hypoadrenocorticism is reported to be more common in female dogs. Houston, Texas •Most cats diagnosed with hyperaldosteronism are male. • Gregory Grauer, DVM, MS, DACVIM Age Predisposition (Internal Medicine) In general, the patient’s age is usually not helpful in determining the specific cause Kansas State University of potassium disorders. Thomas Schermerhorn, VMD, DACVIM ••Diseases that lead to acute or chronic abnormalities of potassium tend to be (Internal Medicine) more common in certain age groups (e.g., chronic renal failure in older cats). Kansas State University ••Hypoadrenocorticism is typically diagnosed in young dogs. The mean age at diagnosis is approximately 4.5 years; roughly 80% of dogs will be <7 years old at diagnosis.

Breed Predisposition ••The majority of hyperaldosteronism cases have been reported in cats, but it is a rare KEY TO COSTS condition; hyperaldosteronism has been reported sporadically in dogs. $ indicates relative costs of any diagnostic and treatment regimens listed. JULY 2003  VOL 5.6

TABLE 1. Mechanisms of Potassium Imbalance

Dietary Mechanisms – The diet is the sole source of body potassium. A change in dietary potassium intake can lead to significant alterations in serum potassium levels. Decreased dietary potassium intake, due to anorexia or chronic GI disease, is a common contributor to the development of in small animal patients, especially cats. due to ingestion of large amounts of potassium is possible but not common.

GI Mechanisms – Potassium is absorbed by the GI tract and is a component of gastric, duodenal, and pancreatic fluid. Large amounts of potassium can be lost in vomitus and in the stool. Chronic GI disease is frequently implicated as a cause of hypokalemia.

Renal Mechanisms – Excess body potassium is principally eliminated via renal excretion. Alterations in the glomerular filtration rate or impaired urine concentration mechanisms can dramatically alter serum potassium concentrations. Regardless of etiology, obstructive uropathy and oliguric/anuric renal failure cause hyperkalemia because renal potassium excretion is decreased. Hypokalemia typically develops in association with diuresis. Osmotic diuresis due to glucosuria, such as occurs in diabetes mellitus, leads to hypokalemia via enhanced renal loss.

Translocation Mechanisms – Nearly all of the body’s potassium pool is mobile, which means that it can shift freely between body compartments (unlike, for example, , which is fixed in the bone pool). There are several well-described physiologic mechanisms for potassium translocation. Acidemia causes hyperkalemia when extracellular hydrogen (H+) are exchanged for intracellular potassium ions (K+); however, caused by organic acids (e.g., lactic acid) does not typically produce clinically significant hyper- kalemia by this mechanism. Conversely, alkalemia produces hypokalemia by the reverse mechanism when extracellular K+ is exchanged for intracellular H+. Any process that produces large movements of water across membranes has the potential to alter serum potassium concentrations, including some metabolic mechanisms. Serum hyperosmolality, for example, produces mild hyperkalemia by this mechanism because it draws intracellular water into the serum; potassium follows water as a consequence of a process known as “solute drag.”

Hormonal Mechanisms – , a produced by the adrenal zona glomerulosa, is the principal that influences serum potassium concentration. Aldosterone is important in blood volume regulation as the effector leg of the renin–angiotensin– aldosterone system. Aldosterone promotes retention and potassium excretion; its major site of action is the distal renal tubules, where it acts to regulate the availability and function of sodium channels. is another hormone that can influence serum potassium concen- trations, although it is not directly involved in potassium regulation. Under the influence of insulin, potassium moves into cells along with and water. The net effect of this translocation process is hypokalemia. This is one of the mechanisms responsible for hypokalemia that develops in treated diabetics and in patients that develop the re-feeding syndrome; the same mechanism is exploited in the treatment of life-threatening hyperkalemia (see Table 3).

Iatrogenic Mechanisms – The use of potassium-containing drugs (e.g., potassium penicillin) and oversupplementation with oral potassium are potential but rare causes of hyperkalemia. An exception is the use of in IV fluids, which can quickly produce hyperkalemia when used in excessive doses or if potassium excretion is impaired (e.g., obstructive uropathy). More commonly, diuresis with potassium-deplete fluids produces hypokalemia. Similarly, the use of potassium-wasting promotes the development of hypokalemia.

••Cats and dogs can develop hypoadrenocorticism, but it is and weakness. Polyuria and polydipsia can occur in association much more common in dogs. Overall, hypoadrenocorticism with hypokalemia (any cause). is an uncommon endocrinopathy. ••Dogs of any breed can develop hypoadrenocorticism, Hyperaldosteronism although certain breeds appear to be more frequently affected ••Cats and dogs exhibit similar clinical signs. than others. Standard poodles (specifically those with a black ••Signs are often episodic; a spectrum of vague signs can be haircoat) are often cited as being predisposed to development reported. of hypoadrenocorticism. Other breeds cited as at risk include ••Polyuria. Labrador retrievers, rottweilers, Great Danes, West Highland ••Polydipsia. white terriers, and Portuguese water dogs. ••Weakness. ••The validity of the apparent breed predispositions is ••Nocturia is an unusual complaint in veterinary medicine that questionable because most cases of hypoadrenocorticism has been reported in several cats with hyperaldosteronism. occur in non-purebred dogs. ••Weight loss. ••Pseudohyperkalemia is a laboratory error detected in hemolyzed ••Ataxia. blood samples. It is most common in Akitas, which have a ••Dysphagia. high potassium concentration in red blood cells. ••Vision loss/blindness. ••Exercise intolerance (reported in a dog with hyperaldosteronism). Owner Observations Owner observations of animals with potassium disorders are Hypoadrenocorticism generally nonspecific; common complaints include lethargy ••Signs are similar in dogs and cats. 2 JULY 2003  VOL 5.6

••Owners are often unaware that the pet is ill until a hypoadrenal ••Marked hypovolemia. crisis develops. ••Abdominal pain. ••Owners often register vague complaints such as lethargy, decreased energy, and reduced activity level. Laboratory Findings ••Signs range in severity from mild to life threatening. Potassium imbalance can occur in association with a large ••Anorexia. number of disorders (Table 2). Discussion of the laboratory ••Weakness. abnormalities that accompany those disorders is beyond the ••GI complaints, such as vomiting/diarrhea/melena. scope of this article. Laboratory findings of primary potassium ••Weight loss. disorders are listed. ••Collapse. Hyperaldosteronism Other Historical Considerations/Predispositions ••Hyperaldosteronemia: Usually marked. The course of illness (acute versus chronic) suggests differential ••Hypokalemia: Marked. diagnoses for potassium abnormalities but is not a reliable ••. diagnostic tool in every circumstance. ••. •Most primary potassium disorders are caused by endocrinop- • ••Elevated (BUN). athies and should be considered when secondary causes of potassium imbalance have been ruled out. Hyperglycemia ••Hypoadrenocorticism in dogs can be part of an endocrinopathy ••Elevated (CK) activity. characterized by multiple endocrine failures, probably from ••Elevated alanine aminotransferase (ALT) activity. an immune-mediated mechanism (autoimmune polyglandular ••Alkalemia. disease). Reported concurrent endocrinopathies include ••Decreased magnesium. hypothyroidism, diabetes mellitus, hypoparathyroidism, and ••Decreased phosphorous. male reproductive failure. ••Elevated bicarbonate. •Increased urinary potassium excretion. Physical Examination Findings • ••Increased fasting plasma renin level. Hypokalemia and hyperkalemia cause very few specific physical abnormalities. Hypoadrenocorticism •Decreased sodium:potassium ratio. Values ≤27 are often cited Hypokalemia of Any Cause • as suspicious for hypoadrenocorticism; values ≤20 are more ••, which can be marked. specific. A low Na/K ratio is not pathognomonic for ••Cervical ventroflexion and inability to raise head is often observed with severe hypokalemia. hypoadrenocorticism because certain nonadrenal disorders ••Muscle weakness of any cause (e.g., myasthenia gravis) may (e.g., severe GI disease) can produce low Na/K ratios. produce similar signs, as can thiamine (vitamin B1) deficiency. ••Hyperkalemia can be marked (many dogs will have K+ ••Cervical ventroflexion due to hypokalemia is flaccid; that concentration >7 mEq/L). produced by thiamine deficiency is spastic. •• can be marked (many dogs will have Na+ concentration <130 mEq/L). Hyperkalemia of Any Cause ••No increase in serum level after adrenocorticotropic ••Lethargy. hormone (ACTH) injection. ••Muscle weakness. ••Mild anemia. ••. ••Mild lymphocytosis, neutropenia, and thrombocytopenia; occasionally eosinophilia or basophilia. Hyperaldosteronism ••Mild hypercalcemia. ••Retinal detachment. ••Mild . ••Weakness (can be marked). ••Azotemia. ••Lethargy. ••. ••Dehydration. ••Hypocholesterolemia. Hypoadrenocorticism ••Hypoproteinemia. ••Bradycardia. ••Animals with atypical hypoadrenocorticism may present with ••Diarrhea. normal electrolyte concentrations. Even with normal ••Melena or hematochezia. , an ACTH stimulation test should be performed ••Poor haircoat. to evaluate adrenal function in animals that have clinical ••Thin body condition. signs that are consistent with hypoadrenocorticism. 3 JULY 2003  VOL 5.6

TABLE 2. Causes of Potassium Imbalance Other Diagnostic Findings Doppler Blood Pressure $ Hyperkalemia ••Hyperaldosteronism is consistently associated with hypertension (>180 mmHg) in cats. • Hypoadrenocorticism (Addison’s Disease). ••Animals presenting with a hypoadrenal crisis often have • Primary : Rare, but reported in dogs and cats. severe hypovolemia and marked hypotension. • Anuric or oliguric renal failure: Any cause. •  (Type 1): Usually present before treat- Ophthalmic Examination $ ment begins. Retinal detachment and hemorrhage is reported in cats with • Renal tubular acidosis (Type 2): Usually develops during treatment. hyperaldosteronism. • Obstructive uropathy: Any cause. • Urinary tract rupture. $ • Metabolic ••Electrocardiography has low sensitivity and high specificity — Metabolic acidosis: Any cause. for hyperkalemia but is generally not helpful for the diagnosis — Exercise in hypothyroid dogs (single report of several cases of hypokalemia. in dogs). ••Hyperkalemia of any cause can produce characteristic ECG — . changes, including: — Trauma (usually severe). — Bradycardia. • Peritoneal effusion. — Wide QRS complex. • (causes pseudohyperkalemia). — Prolonged PR interval. • Thrombocytosis (causes pseudohyperkalemia). — Absence of P waves. Iatrogenic • — Tented T waves. — Oversupplementation of parenteral KCl. — Repeated drainage of chylothorax or cavity effusions. ••Hypokalemia of any cause can produce similar ECG changes: • Drug administration* — Supraventricular and ventricular . — Any potassium-containing drug (e.g., potassium penicillin). — ST segment changes and decreased amplitude can — Beta-adrenergic antagonists. be observed but are inconsistent. — Angiotensin-converting enzyme (ACE) inhibitors. — Prolonged QT interval and the appearance of the U wave — Potassium-sparing diuretics (e.g., ). have been observed with severe hypokalemia (dogs). — NSAIDs. — . Radiography $ • Toxicity ••Radiography has low sensitivity and specificity for the — . diagnosis of primary potassium disorders. — Common oleander (Nerium oleander) toxicity. — Digitalis glycoside toxicity. ••Hyperaldosteronism: Radiographic mass lesions can • Hyperkalemic (single case report in a dog). occasionally be detected in the area of the adrenal glands. ••Hypoadrenocorticism Hypokalemia — Microcardia and a smaller than expected caudal vena cava, due to marked hypovolemia, is commonly observed but is • Primary hyperaldosteronism (reported in cats and dogs). a nonspecific finding. • Chronic renal failure. — Megaesophagus may occur in association with profound • Metabolic — Reduced dietary intake. muscle weakness. — Diabetes mellitus: Hypokalemia may worsened after insulin — Adrenal mass(es) can be observed in animals with treatment. hypoadrenocorticism caused by destructive lesions of the — Metabolic alkalosis: Any cause. adrenal glands (rare). — Re-feeding syndrome. • Protracted vomiting: Any cause. Ultrasonography $$ • Pseudohypoadrenocorticism ••Hyperaldosteronism — Severe GI disease (usually dogs). — Ultrasound examination is more sensitive than radiography — Pregnancy (dogs). for the detection of adrenal pathology. • Iatrogenic — Adrenal mass(es) are detected in most cases. — Diuresis with potassium-deplete fluid. ••Hypoadrenocorticism — Drug administration*: Diuretics (, loop diuretics, — Ultrasonography is generally not useful for the diagnosis osmotic diuretics), and antibiotics (e.g., penicillin, of hypoadrenocorticism. amphotericin B, aminoglycosides). — Finding that the adrenals are very small in size increases Hypokalemic periodic paralysis: Described in Burmese cats. • the suspicion for hypoadrenocorticism but can also be *Modified from Phillips and Polzin, 1998 (see Recommended Reading) caused by prolonged glucocorticoid administration.

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TABLE 3. General Treatment of Potassium Abnormalities

Hypokalemia

Potassium Supplementation Oral supplementation: Oral forms of potassium can be used to treat hypokalemia or supplement potassium intake. Potassium gluconate is the recommended oral supplement. $ • Available in powder, pill, or gel formulations. • Cats: Initially 2–8 mEq/day PO divided bid–tid; maintenance therapy at 2–4 mEq/day (cats). • Dogs: Dogs require 2–44 mEq/L/day depending on size; administer in divided doses as for cats. Recommended starting dose: 5–10 mEq/day with dose adjustments as needed based on serial serum K+ determinations. • Alternative oral formulation is potassium citrate; potassium chloride is not recommended. Parenteral supplementation: Recommended for sick animals or hypokalemic animals that cannot ingest oral supplements. Potassium chloride is routinely used to supplement crystalloid fluids.$ • Available as additive for IV crystalloid fluids. • Depending on the serum potassium concentration, 20–80 mEq of K+ are added to 1 L crystalloid fluid. The following scale is routinely used to determine the amount of potassium to be added to fluids. Serum K+ (mEq/L) Amount K+ added to fluid (mEq/L) 3.5–4.5 20 3.0–3.5 40 2.5–3.0 60 2.0–2.5 80 • As a rule of thumb, the rate of parenteral potassium supplementation should not exceed 0.5 mEq/kg/hr. • Potassium supplementation is contraindicated in patients with hyperkalemia or impaired potassium excretion. • Potassium may be substituted to provide simultaneous phosphate supplementation.

Hyperkalemia

Assess the need for specific therapy of hyperkalemia. Not all circumstances require specific measures to treat hyperkalemia (e.g., moderate hyperkalemia in a cat with lower urinary tract obstruction may resolve with relief of the obstruction and fluid diuresis). Hyperkalemia that is causing cardiac or ECG changes should be treated. If specific treatment is needed: • Address any underlying cause. • Diuresis: Administer crystalloid fluid (e.g., 0.9% NaCl) IV to achieve diuresis. The rate of fluid administration will depend on the patient’s volume status and cause of the hyperkalemia. $ • Consider using a specific treatment to lower potassium: — 10% , 0.5–1.0 mL/kg IV slowly over 2–4 minutes; monitor the ECG during infusion. The principal effect is cardioprotection; it is indicated when cardiac consequences of hyperkalemia are imminent. $ — , 0.1 U/kg IV followed by 1–2 g of 50% dextrose/unit of insulin IV (the dextrose solution should be diluted to 10%). Dextrose should be added to IV fluids to prevent hypoglycemia.$ — Dextrose bolus alone (without exogenous insulin) may be used to treat moderate hyperkalemia. 50% dextrose is diluted to 10% prior to infusion. Dextrose should be added to IV fluids to prevent hypoglycemia.$ — , 1–2 mEq/kg IV slowly (can be repeated if necessary). This treatment may be especially useful in patients with concurrent acidosis.

Summary of Diagnostic Criteria ••Hypoadrenocorticism ••Laboratory confirmation of serum potassium levels below —The combination of hypocortisolemia and lack of adrenal (hypokalemia) or above (hyperkalemia) the reference range is response to stimulation by ACTH is diagnostic. sufficient for diagnosis of a potassium disorder. —Hyponatremia with hyperkalemia (low Na/K ratio) is ••Hyperaldosteronism often present. — Hyperaldosteronemia in the absence of diseases that cause a secondary increase in aldosterone (e.g., failure). Differential Diagnoses — Concurrent hypokalemia and hypertension, with appropriate Potassium abnormalities occur as a secondary of clinical signs. many different diseases as well as a result of primary disorders —An adrenal mass is usually present in dogs and cats. of potassium homeostasis. The differential diagnoses for

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Iatrogenic Hyperkalemia RESOURCE LIST ••Excessive administration of potassium-containing drugs or • Synthetic ACTH (Cortrosyn, Organon): 0.25 mg/dog IM. fluids. Measure pre- and 1-hour post-injection cortisol level. ••Peritoneal/pleural fluid drainage. Commercial availability may be sporadic in the future. Factitious Hyperkalemia • Regular insulin (Humulin R, Eli Lilly): 0.1 U/kg IV followed Laboratory artifact caused by thrombocytosis or hemolysis. by dextrose bolus as treatment for acute hyperkalemia. • 50% dextrose solution: 1–2 g of dextrose/unit of insulin IV TREATMENT RECOMMENDATIONS (dilute to a 10% dextrose solution for administration). • Potassium gluconate (Tumil-K, King Animal Health): Initially Initial Treatment 2–8 mEq/day PO divided bid–tid; maintenance therapy General treatments for potassium disorders are shown in Table 3. at 2–4 mEq/day (cats). Dogs require 2–44 mEq/L/day Specific therapy for primary potassium disorders is outlined depending on size; administer in divided doses as for below. cats. Recommended starting dose: 5–10 mEq/day with Hyperaldosteronism dose adjustments as needed based on serial serum K+ ••Restore normokalemia using potassium supplementation (see determinations. Table 3). • Potassium chloride for injection: Add 20–80 mEq/L to IV ••Control hypertension. fluids for parenteral potassium supplementation. ••Adrenalectomy to remove aldosteronoma. • Fludrocortisone acetate (Florinef Acetate, King Hypoadrenocorticism Pharmaceuticals): Initial dose of 0.01–0.02 mg/kg PO Supportive care to reduce hyperkalemia (see Table 3). once daily; adjust by 0.005–0.01 mg increments as •• •Mineralocorticoid supplementation: needed to control electrolyte abnormalities. • — Desoxycorticosterone pivalate (DOCP), 2.2 mg/kg IM • Prednisone: 0.1–0.25 mg/kg PO bid prn for glucocorticoid every 21 to 30 days. The authors generally do not exceed a replacement. total dose of 50 mg/injection; this dose is generally • Desoxycorticosterone pivalate (DOCP; Percorten-V, efficacious for large dogs, even those >50 kg. Adjustments Novartis): 2.2 mg/kg IM every 21–30 days. Do not in the administered dose are made based on electrolyte exceed a total dose of 50 mg/injection. concentrations (measured 10 to 14 days after the injection • 10% calcium gluconate solution: 0.5–1.0 mL/kg IV slowly for the initial 2 to 3 injections), and the frequency is over 2–4 minutes. adjusted based on the duration of the injection. Dose adjustments, when made, are usually small changes (10% increase or decrease) and are reflected in the next injection hyperkalemia and hypokalemia are shown in Table 2. Common (e.g., a dog that has hypokalemia on day 14 will receive diseases and disorders associated with potassium abnormalities 10% less DOCP at the next treatment). Most dogs will be that resemble those caused by primary potassium disorders are controlled with a DOCP injection every 3 to 4 weeks. discussed below. — Fludrocortisone, initial dose of 0.01 to 0.02 mg/kg PO once daily; adjust in increments of 0.05 to 0.1 mg per day Hyperaldosteronism as needed to control electrolyte abnormalities. ••Renal failure is differentiated by laboratory evaluation and ••Glucocorticoid replacement: Prednisone, 0.2 mg/kg PO to response to IV fluid therapy. provide exogenous glucocorticoids if needed. Usually ••Normal ACTH stimulation with hypoaldosteronemia. required when DOCP is used; may not be needed if fludro- cortisone is used as this drug also has glucocorticoid activity. Hypoadrenocorticism The dose of prednisone should be increased when stressful ••Pseudohypoadrenocorticism: Affected animals have a normal events are anticipated. ACTH stimulation. ••Severe GI disease: GI diagnostics, including fecal examination. Patient Monitoring ••Pregnancy: Documentation of pregnant state. ••Serial determination of serum electrolytes is indicated for all ••Any cause of impaired renal potassium excretion. animals treated for potassium disorders until the electrolytes — Acute renal failure: Normal ACTH stimulation. are normal and the patient’s condition is stable. Electrolytes — Obstructive uropathy (any cause). should be measured every 6 to 24 hours depending on the — Severe hypovolemia or other cause of marked reduction in patient’s condition and the expected rate of change in the renal blood flow. electrolytes.

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••Resolution of clinical signs should accompany correction of PROGNOSIS electrolytes. ••ECG monitoring is important for assessment of hyperkalemic Favorable Criteria patients and during the treatment of hyperkalemia with ••Correctable/reversible cause of hypo- or hyperkalemia. calcium gluconate (see Table 3). ••Hyperaldosteronism: Adrenal mass identifiable and amenable ••Efficacy of mineralocorticoid treatment of animals with to surgical removal. hypoadrenocorticism is monitored using serial measurements ••Hypoadrenocorticism: of serum sodium and potassium concentrations. Initially, — Rapid recognition and diagnosis of clinical signs. electrolytes are monitored every 1 to 2 weeks. Once electrolyte — Patient does not have renal failure. concentrations are stable, monitoring every 3 months may be — Electrolyte concentrations readily controlled with appropriate. mineralocorticoid supplementation. Home Management Unfavorable Criteria Hyperaldosteronism and Hypoadrenocorticism ••Cause of hypo- or hyperkalemia is not reversible or readily ••Owner compliance with prescribed treatments must be treated. encouraged to avoid recurrence of clinical signs. ••Treatment failure or poor response. Alternative therapy ••Owners must be educated about the expected clinical signs should be attempted if a patient fails to respond to initial that may occur if treatment fails or the problem recurs. therapeutic attempts. ••The need for periodic examination by a veterinarian must be ••Hyperaldosteronism: emphasized, especially in animals with hypoadrenocorticism — Patient is a poor surgical candidate. that must receive life-long therapy. — Adrenal mass is not resectable or has invaded the caudal vena cava. Milestones/Recovery Time Frames — Irreversible or debilitating complications of hypertension Hyperaldosteronism occur (e.g., neurologic deficits). ••Resolution of serum electrolyte and hormone abnormalities ••Hypoadrenocorticism: should occur within 24 to 36 hours following surgical — Megaesophagus does not resolve with hormone treatment removal of aldosteronoma. or aspiration pneumonia is present. ••Resolution of clinical signs should parallel normalization of — Patient has renal failure. electrolyte concentrations. — Patient has secondary hypoadrenocorticism, which can be associated with less favorable prognosis than primary Hypoadrenocorticism hypoadrenocorticism, depending on the initiating cause. ••Dramatic improvement in clinical and laboratory abnormalities — Poor control of electrolytes with . can be observed after volume replacement alone, but — Cost of treatment is prohibitive for the pet owner. complete resolution will not occur until proper hormonal therapy is begun. ••Glucocorticoid therapy is responsible for alleviation of many RECOMMENDED READING of the most dramatic clinical signs (profound lethargy, GI DiBartola SP, Autran de Morais H: Disorders of potassium, signs, and vascular collapse). in DiBartola SP (ed): Fluid Therapy in Small Animal Practice. ••Electrolyte disturbances may not completely resolve until Philadelphia, WB Saunders, 2000, pp 83–107. mineralocorticoid therapy is instituted. Feldman EC, Nelson RW: Hypoadrenocorticism, in Feldman Treatment Contraindications EC, Nelson RW (eds): Canine and Feline Endocrinology and Reproduction. Philadelphia, WB Saunders, 1996, pp Hypokalemia 266–305. ••Potassium chloride is contraindicated as an oral potassium supplement because it is not well tolerated; use can cause Flood SM, Randolph JF, Gelzer AR, Refsal K: Primary hyperal- dosteronism in two cats. J Am Anim Hosp Assoc 35(5):411– vomiting and promote acidosis. 416, 1999. Hyperkalemia Phillips SL, Polzin DJ: Clinical disorders of potassium homeostasis. ••Potassium supplementation by any method is contraindicated Vet Clin North Am Small Anim Pract 28(3):545–564, 1998. if hyperkalemia is suspected or documented. Potassium- sparing diuretics are contraindicated.

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